1,354,484 research outputs found
TRPA1 and cold transduction: An unresolved issue?
No full textTRPA1 was originally characterized as a cold-activated ion channel; however, since the initial description there has been some disagreement about its role in cold sensation. Here, we review the literature on the function of TRPA1 as a cold sensor. Many studies have demonstrated that TRPA1 can be activated by cold when expressed in heterologous systems, but its role as a cold sensor in native peripheral sensory neurons remains uncertain. We argue that TRPA1 is activated indirectly by cold via a background Ca 2+ infl ux seen in cells during cooling. This background cold response is present in most heterologous cell types, but not in sensory neurons. Thus, we propose that cold sensitivity of TRPA1 is indirect and is dependent on cellular context. © 2009 Caspani and Heppenstall
Heppenstall, C R, 47022
No full textThis record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/391889Surname: HEPPENSTALL. Given Name(s) or Initials: C R. Military Service Number or Last Known Location: 47022. Missing, Wounded and Prisoner of War Enquiry Card Index Number: SEA-3942.209306
Item: [2016.0049.24182] "Heppenstall, C R, 47022
A role for T-type Ca2+ channels in mechanosensation
No full textPrimary afferent sensory neurons were amongst the first neuronal cell types to be studied for the expression of low-voltage-activated Ca2+ currents. Many early studies took advantage of the fact that these neurons are relatively easy to isolate and record from, and much of the initial biophysical data on T-type Ca2+ channels came from cultured sensory neurons [1-5]. Shortly after this current had been described in sensory neurons, it was realized that the expression of T-type current is not constant across the DRG but appears to differ amongst subsets of sensory neuron [6]. It was suggested that these channels might contribute to particular sensations transmitted by individual neurons and this has recently been put to the test using pharmacological and genetic experiments in animal models of pain and mechanosensation. © 2006 Elsevier Ltd. All rights reserved
Mrs. Heppenstall, a member of the Chapman family, Abington, Illinois
No full textCabinet card photographic portrait of Nancy Wallace Pearson Heppenstall [1834-1916], taken in the studio of William Johnston, Abington, Illinois. She was the mother of Lizzie Pearson Chapman, wife of Charles Clarke Chapman.https://digitalcommons.chapman.edu/chapman_family/1077/thumbnail.jp
Neurotrophins, nociceptors and pain
No full textNerve growth factor (NGF) is known to play a key role in the development of hyperalgesia after inflammatory injury. The increased levels of NGF that accompany injury lead to hyperalgesia via peripheral and central spinal mechanisms. New evidence reviewed here indicates that NGF can directly sensitize nociceptive neurones to noxious heat stimuli through rapid modulation of heat/vanilloid receptors or via de-novo increased expression of heat receptors. In addition, new data suggest that the central sensitization that can result from increased NGF may be mediated via central release of another neurotrophin, brain-derived neurotrophic factor. (C) 2000 Lippincott Williams and Wilkins
BDNF but not NT-4 is required for normal flexion reflex plasticity and function
No full textNeurotrophins can directly modulate the function of diverse types of central nervous system synapses. Brain-derived neurotrophic factor (BDNF) might be released by nociceptors onto spinal neurons and mediate central sensitization associated with chronic pain. We have studied the role of BDNF and neurotrophin-4 (NT-4), both ligands of the trkB tyrosine kinase receptor, in synaptic transmission and reflex plasticity in the mouse spinal cord. We used an in vitro spinal cord preparation to measure monosynaptic and polysynaptic reflexes evoked by primary afferents in BDNF- and NT-4-deficient mice. In situ hybridization studies show that both these neurotrophins are synthesized by sensory neurons, and NT-4, but not BDNF, also is expressed by spinal neurons. BDNF null mutants display selective deficits in the ventral root potential (VRP) evoked by stimulating nociceptive primary afferents whereas the non-nociceptive portion of the VRP remained unaltered. In addition, activity-dependent plasticity of the VRP evoked by repetitive (1 Hz) stimulation of nociceptive primary afferents (termed windup) was substantially reduced in BDNF-deficient mice. This plasticity also was reduced in a reversible manner by the protein kinase inhibitor K252a. Although the trkB ligand NT-4 is normally present, reflex properties in NT-4 null mutant mice were normal. Pharmacological studies also indicated that spinal N-methyl-o-aspartate receptor function was unaltered in BDNF-deficient mice. Using immunocytochemistry for markers of nociceptive neurons we found no evidence that their number or connectivity was substantially altered in BDNF-deficient mice. Our data therefore are consistent with a direct role for presynaptic BDNF release from sensory neurons in the modulation of pain-related neurotransmission
Breaking the pain barrier
No full textArtemin reverses pain and neurochemical changes after nerve injury in an animal model. The molecule could potentially treat neuropathic pain, in which even the slightest touch can hurt (pages 1383-1389)
Glycine receptor regulation of neurokinin receptor function, in rat dorsal horn neurones
No full textACTIVATION of spinal neurokinin (NK1) receptors leads to increases in the extracellular concentration of glycine in the dorsal horn. We have investigated the role of the inhibitory glycine receptor as a regulator of NK1 receptor-mediated effects on dorsal horn neurones. Ionophoretic application of GR82334, a selective NK1 antagonist, did not alter dorsal horn neuronal activity evoked by cutaneous applications of mustard oil. However, in the presence of the glycine antagonists, strychnine or phenylbenzene-ω-phosphono-α-amino acid (PMBA), GR82334 displayed inhibitory properties. Therefore inhibitory glycine receptors may mask the contribution made by NK1 receptors to nociceptive processing. This is discussed with reference to the role of NK1 receptors during brief and long duration nociceptive transmission
TrkC-CreERT2-mediated recombination supports evidence that TrkC+/TH+ DRG neurons contribute to cardiovascular homeostasis
No full textIn their Matters Arising article, McMullan et al. (2022) offer alternative explanations for the phenotypes we observed upon stimulation and ablation of TrkCCreERT2-positive neurons in mice. Their interpretations are focused on two aspects: first, whether the vasoconstriction we observed upon activation of TrkCCreERT2 neurons is really mediated by TrkC/TH-positive neurons, or whether it might stem from stimulation of somatic nociceptors that also express TrkC; and second, whether the lethality observed after ablation of TrkCCreERT2 neurons might be a result of ablation of vagal afferents and not TrkC/TH neurons located in the spinal ganglia. Central to both of these concerns is the expression and recombination efficiency of the TrkCCreERT2 transgene in these other cell types. This Matters Arising Response paper addresses the McMullan et al. (2022) Matters Arising paper, published concurrently in Cell Reports
An Evaluation of Edward Heppenstall\u27s Doctrine of Redemption
No full textOne of the major problems in the study of the doctrine of redemption is that it has been linked to the cross while overlooking its etiological and eschatological perspectives. This has caused many to dissociate creation and redemption, leading to the acceptance of an evolutionistic approach to theology, and redemption and eschatology, leading to the mitigation of the connection of the two in the New Testament.
While other Christian traditions emphasize the atoning death of Christ, Adventist theology has tended to overemphasize its eschatological significance. Thus, in Adventism, there is need to present a more balanced view of redemption. Edward Heppenstall was chosen as the subject of this dissertation since he more comprehensively deals with this doctrine.
Factors that shaped Heppenstall\u27s particular understanding of redemption are presented in a brief biographical, historical, and theological overview in chapter 1. His view on the scope and the need of redemption, the nature of man, and sin are discussed in chapter 2. Chapters 3 through 6 encompass Heppenstall\u27s scheme of redemption, namely: its promise, its act and results, and its work of judgment. Each chapter analyzes the way Heppenstall links God, sin, law and covenant, Christology, salvation, and eschatology to his general view of redemption. In chapter 7, a comparison of his understanding of redemption is made to the views of other Adventist writers and with E. G. White.
The final chapter evaluates the strengths and weaknesses of Heppenstall\u27s model for describing redemption. It was noted that he did not develop a biblical foundation to support his view of the great controversy. However, it was found that this motif is a valid biblical model for understanding the doctrine, since it forms an adequate foundation for a more comprehensive view of redemption. In relationship to his theology of redemption, it was pointed out that he gave little attention to some aspects of anthropology, and ecclesiology. At the same time serious questions are raised concerning his understanding of some aspects of the doctrine of the sanctuary. Positively, Heppenstall introduced new aspects in the biblical concept of the covenant and reemphasized some neglected aspects in the understanding of law, Christology, soteriology, and the sanctuary doctrine
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